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61,005 resultsShowing papers similar to Synergistic neurotoxicity of polystyrene nanoplastics and cadmium co-exposure: oxidative stress, mitochondrial dysfunction, and ATF5-mediated mitochondrial unfolded protein response in C. elegans and PC12 cells
ClearPolystyrene exacerbates cadmium‐induced mitochondrial damage to lung by blocking autophagy in mice
Researchers found that polystyrene microplastics exacerbated cadmium-induced mitochondrial damage in mouse lungs by blocking autophagy, revealing a synergistic toxicity mechanism when these two common environmental contaminants co-occur.
Redefining the synergistic toxicity of nano-plastics and cadmium in earthworm coelomocytes: the mechanism of α-amylase molecular docking orientation and energy crisis
Researchers exposed earthworm immune cells (coelomocytes) to polystyrene nanoplastics combined with the heavy metal cadmium, finding that nanoplastics act as carriers that amplify cadmium uptake and worsen oxidative stress, energy metabolism disruption, and enzyme damage beyond what cadmium causes alone.
Maternal Exposure to Combined Cadmium and Polystyrene Nanoplastics Induces Offspring Testicular Dysplasia via Mitochondrial Reactive Oxygen Species Overactivating the Peroxisome Proliferator-Activated Receptor α-Mediated Autophagy Signaling Pathway
Researchers investigated the combined effects of maternal exposure to polystyrene nanoplastics and cadmium on offspring in a mouse model. The study found that co-exposure caused testicular developmental abnormalities in offspring through mitochondrial oxidative stress and disrupted autophagy signaling, suggesting that nanoplastics may amplify the reproductive toxicity of co-occurring environmental contaminants.
The joint effects of nanoplastics and TBBPA on neurodevelopmental toxicity inCaenorhabditis elegans
Researchers used the model organism C. elegans to study the combined neurodevelopmental effects of polystyrene nanoplastics and the flame retardant TBBPA. The study found that combined exposure produced synergistic harmful effects including reduced survival, impaired movement, oxidative stress, and dopaminergic neuron loss, with specific genes related to neurodegenerative pathways playing key roles in the observed toxicity.
Synergistic effects of PS-NPs and Cd on ovarian toxicity in adolescent rats: Ferroptosis by induction of mitochondrial redox imbalance via the SIRT3-SOD2/Gpx4 pathway
Researchers studied the combined effects of polystyrene nanoplastics and cadmium on the ovaries of adolescent rats over 28 days. They found that co-exposure was significantly more harmful than either pollutant alone, causing damage to ovarian structure and hormone disruption through a process called ferroptosis triggered by mitochondrial oxidative stress. The study suggests that nanoplastics may act as a carrier that amplifies heavy metal toxicity to the reproductive system during critical developmental periods.
Maternal Exposureto Combined Cadmium and PolystyreneNanoplastics Induces Offspring Testicular Dysplasia via MitochondrialReactive Oxygen Species Overactivating the Peroxisome Proliferator-ActivatedReceptor α‑Mediated Autophagy Signaling Pathway
Maternal exposure to combined polystyrene nanoplastics and cadmium during pregnancy caused testicular dysplasia in offspring via mitochondrial reactive oxygen species overactivating the PPARα-mediated autophagy pathway, with combined exposure more harmful than either alone.
Exploring the mechanisms of neurotoxic effects from combined exposure to polystyrene and microcystin-LR in Caenorhabditis elegans
Researchers studied the combined neurotoxic effects of polystyrene microplastics and the cyanotoxin microcystin-LR in an animal model, finding synergistic damage to brain tissue through oxidative stress and neuroinflammation pathways beyond what either contaminant caused alone.
Co-exposure to environmentally relevant concentrations of cadmium and polystyrene nanoplastics induced oxidative stress, ferroptosis and excessive mitophagy in mice kidney
A mouse study found that combined exposure to cadmium (a toxic metal) and polystyrene nanoplastics caused more kidney damage than either pollutant alone. The combination triggered a harmful chain reaction involving oxidative stress, iron buildup, and excessive breakdown of cellular energy factories called mitochondria. This is significant because people are often exposed to both nanoplastics and heavy metals simultaneously, and their combined effects may be worse than expected.
Toxicity induction of nanopolystyrene under microgravity stress condition in Caenorhabditis elegans.
This study used Caenorhabditis elegans to examine how nanopolystyrene exposure interacts with microgravity stress, finding that nanoplastic exposure amplified the toxicity of simulated weightlessness. The combined stress increased oxidative damage and triggered mitochondrial stress responses, suggesting that nanoplastics can worsen the effects of other environmental stressors.
Polystyrene Nanoplastics and Cadmium Co-Exposure Accelerates Mitochondrial Autophagy Mediated by HSP60–SIRT3–SOD 2 Signaling Pathway in Primary Duck Embryo Hepatocytes
Scientists found that when tiny plastic particles and the toxic metal cadmium are combined, they cause more damage to liver cells than either pollutant alone. The plastic particles help cadmium get into cells more easily, leading to harmful changes in the cell's powerhouses (mitochondria) and increased cell death. While this study used duck cells, it suggests that the growing presence of microplastics in our environment could make heavy metal pollution more dangerous to human health.
Co-exposure of cadmium and polystyrene nanoplastics: Induction pyroptosis and autophagy in mice testis
Researchers investigated the combined effects of cadmium and polystyrene nanoplastics on mouse testicular tissue. The study found that co-exposure produced more severe testicular damage than either substance alone, driven by the interplay between pyroptosis (inflammatory cell death) and autophagy. Inhibiting one of these cellular processes affected the other, suggesting they are closely interconnected in the toxicity response to nanoplastic and heavy metal co-exposure.
The mechanism of oxidative stress induced by nanoplastics in Caenorhabditis elegans: Integrated analysis of transcriptomics and metabolomics
Researchers exposed C. elegans nematodes to polystyrene nanoplastics across a concentration range and integrated transcriptomic and metabolomic data to identify disrupted fatty acid and glutathione metabolism as the central drivers of oxidative stress, with the gene gst-4 and specific metabolites serving as key molecular signatures.
Environmental Concentrations of Polystyrene Nanoplastics Induce Low‐Dose Tamoxifen Toxicity Through Oxidative Stress in Caenorhabditis elegans
Researchers used the model organism C. elegans to investigate how environmental concentrations of polystyrene nanoplastics interact with the cancer drug tamoxifen. Combined exposure significantly impaired locomotion, reproduction, and growth while inducing oxidative stress through the DAF-2/DAF-16 insulin signaling pathway. The study suggests that long-term exposure to environmental levels of nanoplastics could enhance the side effects of pharmaceutical drugs in living organisms.
Mitochondrial dysfunction and lipometabolic disturbance induced by the co-effect of polystyrene nanoplastics and copper impede early life stage development of zebrafish (Danio rerio)
Researchers found that co-exposure to polystyrene nanoplastics and copper at environmentally relevant concentrations caused mitochondrial dysfunction and lipid metabolism disruption in zebrafish embryos, impairing early development and survival more severely than either contaminant alone.
Combinational effect of titanium dioxide nanoparticles and nanopolystyrene particles at environmentally relevant concentrations on nematode Caenorhabditis elegans
Researchers exposed the model nematode Caenorhabditis elegans to environmentally realistic concentrations of both titanium dioxide nanoparticles and nanopolystyrene simultaneously, finding that nanoplastics enhanced the toxicity of the metal oxide particles, worsening locomotion impairment and gut oxidative stress beyond what either pollutant caused alone.
Adverse effects of polystyrene nanoplastic and its binary mixtures with nonylphenol on zebrafish nervous system: From oxidative stress to impaired neurotransmitter system
Researchers investigated the individual and combined effects of polystyrene nanoplastics and the industrial chemical nonylphenol on the zebrafish nervous system over 45 days. Both substances induced oxidative stress and disrupted neurotransmitter systems, with combined exposure generally producing more severe effects on glutamate metabolism and brain tissue damage. The study suggests that the interaction between nanoplastics and co-occurring environmental pollutants can amplify neurotoxic effects in fish.
Polystyrene nanoparticles cause dynamic alteration in mitochondrial unfolded protein response from parents to the offspring in C. elegans
Researchers investigated how polystyrene nanoparticles affect the mitochondrial stress response across generations in C. elegans nematodes. The study found that nanoparticle exposure suppressed the mitochondrial unfolded protein response in a dose-dependent manner from parents through to the second offspring generation, indicating that parental plastic exposure can compromise the cellular stress defenses of future generations.
Combinational exposure to hydroxyatrazine increases neurotoxicity of polystyrene nanoparticles on Caenorhabditis elegans
Researchers used C. elegans worms to show that hydroxyatrazine (a common herbicide metabolite) amplifies the neurotoxicity of polystyrene nanoparticles at environmentally relevant concentrations, triggering motor neuron degeneration and altered movement behavior through genes governing neuronal calcium signaling and cell death.
Polystyrene nanoplastics at predicted environmental concentrations enhance the toxicity of copper on Caenorhabditis elegans
Even at low concentrations found in the environment, polystyrene nanoplastics significantly increased copper toxicity in roundworms by boosting oxidative stress and triggering stress-response genes. The nanoplastics alone did not cause obvious harm, but when combined with copper, the damage was much worse than copper alone. This is concerning because in real-world soil and water, nanoplastics and heavy metals often occur together, potentially creating greater health risks than either pollutant individually.
Intestinal mitochondrial unfolded protein response induced by nanoplastic particles in Caenorhabditis elegans
Nanopolystyrene exposure in C. elegans activated the mitochondrial unfolded protein response (mtUPR) in intestinal cells at concentrations of 1–100 µg/L, and knockdown of the protective chaperone hsp-6 increased susceptibility — identifying mtUPR as a key stress response pathway for nanoplastic toxicity.
Synergistic effect of PS-MPs and Cd on male reproductive toxicity: Ferroptosis via Keap1-Nrf2 pathway
A mouse study found that microplastics and the heavy metal cadmium work together to cause more severe damage to male reproductive organs than either pollutant alone. The combination triggered a form of cell death called ferroptosis by disrupting a key protective pathway in the body. This is the first study to show this synergistic reproductive harm, suggesting that microplastics can make other environmental toxins more dangerous.
Joint toxic effects of polystyrene nanoparticles and organochlorine pesticides (chlordane and hexachlorocyclohexane) on Caenorhabditis elegans
Joint exposure to polystyrene nanoplastics and organochlorine pesticides (chlordane and HCH) in the roundworm C. elegans caused greater toxicity than either pollutant alone, suggesting synergistic interactions. These findings highlight the importance of studying combined pollutant effects rather than individual chemicals in isolation.
The role of Sod-2 in different types of neuronal damage and behavioral changes induced by polystyrene nanoplastics in Caenorhabditis elegans
Researchers used the roundworm C. elegans to study how polystyrene nanoplastics damage the nervous system at concentrations found in agricultural soils. They found that the nanoplastics caused nerve damage in a specific order, first affecting dopamine neurons, then acetylcholine neurons, and finally GABA neurons, through a process involving oxidative stress and reduced antioxidant protein levels. The study identifies a specific cellular pathway through which nanoplastics cause neurotoxic effects, and shows that a mitochondrial antioxidant could help alleviate the damage.
Effects of chronic co-exposure polystyrene nanoplastics and cadmium on liver function in Prussian carp (Carassius gibelio)
Researchers exposed Prussian carp to polystyrene nanoplastics and cadmium, both individually and together, for 21 days and found that the combination caused significantly worse liver damage than either pollutant alone. The nanoplastics enhanced cadmium accumulation in the liver and amplified oxidative stress, tissue damage, and immune gene activation. The findings demonstrate that nanoplastics and heavy metals can have synergistic toxic effects on aquatic organisms.